Micro Flashcards
(80 cards)
1
Q
structure of herpes virus
A
iscosahedral capsid
lipid envelope
~dozen virus-encoded glycoproteins
2
Q
what is the tegument of a herp virus?
A
- bw capsid and envelope
- location of proteins needed for infection, rep
3
Q
which herp type is the biggest?
A
CMV
[cause its mega]
4
Q
what is the genome of herp like?
A
large
DS DNA
150-250 kb pairs
5
Q
where does replication of herp genome take place?
A
nucleus of host cell
6
Q
what type of inf does herp ususally cause? what is the exception to this?
A
- self limiting, no symptoms
- exception for immunocompromised pt, Cx and life-threatening inf
7
Q
what kind of replication does herp have?
A
lytic
8
Q
name the overall stages of herp infection:
A
I. attachment and entry II. production of IE proteins III. E proteins IV. L proteins V. exit
9
Q
what are the three herp virus types Ryan taught us? where are they hibernate/latetent?
A
EBV
CMV
HH8/KHSV
lymphocyte
10
Q
describe the attachment and entry phase
A
- virus attaches to heparan sulfate proteoglycans
- nucleocapsid is released
- migrates in on microtubule
- goes to nucleus
- barfs genetic material into nucleus
11
Q
what is special about virus entry into the cell?
A
- fuses directly with p.m. bc both lipid
- pH INdependent woman
12
Q
word association time: intermediate-early protein
A
Tx factors (viral) RNAp II (host): directed to viral expression
13
Q
word association time: early protein
A
replication/non-structural proteins
DNAp (viral)c
thymidine kinase
14
Q
word association time: late protein
A
structural proteins
capsid, glyco proteins
15
Q
where does packaging of new nuclear material occur?
A
nucleus of host cell
16
Q
why is this called a cascade expression? what steps does intermediate-early drive?
A
- because one step starts the next step
- early AND late
17
Q
path of packaged virus’ exit from cell
A
ER –> golgi –> p.m. –> buds off in fully-enveloped
18
Q
what is the importance of thymidine kinase?
A
- phosphorylates a variety of NT besides thymidine
- point of drug Tx
19
Q
what is key about latency?
A
- all herps do it
- entire genome maintained
- NO VIRUSES PRODUCED
20
Q
what genes are active in latency?
A
only the ones needed to maintain latency
:: more expressed in the lymphotrophic viruses than CNS-trophic
21
Q
what are the three stages of latency?
A
- establishment
- maintenance
- reactivation
22
Q
describe genome structure of HSV-1 or -2
A
- unique-long (UL), unique-short (US) flanked by inverted repeat-long (IRL) and inverted repeat-short (IRS)
- unique has single copy of each gene
- IR are identical sequences but in opposite orientation :: have 2 copes per IR
23
Q
describe the genome structure of EBV
A
- multiple internal repeats
- same direction
- amplification
24
Q
describe the genome structure of HCMV
A
same as HSV 2 U and 2 IR
25
when does reactivation occur?
when there is a lapse in immunity
26
what is the part of latency that causes Cx, sequelae, etc - the fact that you have it for life or the fact that you have recurrent infections?
having it for life
27
what are the three genome classes of heps? what are their top members? where are they latent?
- alpha: CNS-tropic; HSV-1 and -2, varicella
- beta: lymphotropic; CMV, HHV-6, HHV-7
- gamma: lymphotropic; EBV, HHV-8
28
what do the beta and the gamma have inc common?
both lymphotropic
29
word association: Acyclovir
```
prodrug
thymidine kinase (virus)
```
30
word association: Ganciclovir
analog
| CMV
31
word association: Foscarnet
pyrophosphate analog
| backup Tx
32
word association: Cidofovir
citadine analog
| DNAp inhibitor
33
CMV (is/is not) highly contagious
is NOT
34
CMV incidence is increased in what population?
adult
low SES: 80%
higher SES: 50%
35
CMV infection occurs when?
low SES: 1-2 YO
| higher SES: 16 YO
36
what is CMV found in? so who does this put at risk?
saliva, urine, breast milk, semen, cervical secretions, blood/transplanted organs
neonates, day care workers, immunicomprimised pts, gay men
37
how do you get CMV?
direct contact with secretions
38
what cells does CMV infect? what does CMV look like under the microscope?
Bcells
Tcells
monocytes
lymphoctes
large, puffed-up cells
39
what can neonatal CMV infections result in? what about adult?
fetuses: most asymptomatic, but can cause retardation and deafness!
adults: mono with fever
40
who is esp at risk for CMV? what are the vehicles of transmission?
AIDS, transplant pts**
AIDS - sexytime
transplant - (+) donor gives to (-) recipient or latent in recipient is reactivated when immunosupressed for Sx
41
CMV AIDS pts are esp at risk of
retinitis
42
what commonly presents with CMV organ transplant pts?
pneumonia 1-4 mo after Sx, preceded by fever
43
how do you diagnose CMV?
ELISA
PCR
Shell assay (24h)
44
what is the Rx of choice for CMV?
Ganciclovir
45
what are side effects of Ganciclovir?
neutropenia
| GI bleeding
46
EBV infection occurs when?
low SES: early age
| higher SES: adolescence, early adult hood (when people start kissing)
47
hoe much of the adult population has ENV Ab?
90-95%
48
what can EBV cause in immunnocomp pts?
oral hairy leukoplakia (on tongue)
mostly AIDS pts
49
what can you Tx oral hairy leukoplakia with? but what happens when you stop Tx?
acyclovir
comes back
50
oral hairy leukoplakia is caused by active/latent EBV
active
51
what is PTLD?
post-transplant lymphoproliferative disease from EBV
52
EBV is assoc with what diseases?
PTLD
nasopharyngeal carcinoma
Burkitt's lymphoma
53
what is the incubation time for EBV? what is its path through the body?
7 wks
| oropharyngeal epithelium --> lymphocytes --> liver --> spleen
54
where is EBV latent?
throat epithelium
| B-cells
55
how long is EBV "shed"? where is it shed from?
sheds for weeks
| oral shedding
56
symptoms for EBV
mostly asymptomatic
| infectious mononucleosis
57
diagnosing EBV
- 50% atypical, large lymphocytes
lobulated nuclei
- antigenic markers
- heterophile Ab aka Monospot Test
58
what is notable about the microscopic presentation of EBV?
the cells that are fat are Tcells responding to the infected Bcells
59
what are the antigenic markers for EBV? what do they mean?
EBNA, VCA
primary infection: anti-VCA IgM (+)
primary infection: anti-VCA IgG (+), anti-EBNA (-)
past/resolved inf: anti-VCA IgG (+), anti-EBNA IgG (+)
60
what is a (+) result in the Monospot Test? what does it rule in or out?
sign: agglutination of sheep RBC
(+): def EBV mono
(-): could be EBV or CMV mono
61
what is the mechanism in PTLD? how do you treat it?
Bcells proliferating without CTLs to control them
| Tx by stopping immunosupression
62
what Rx is not useful in PTLD? why?
Ancyclovir
| bc virus latent
63
what is Burkitt's Lymphoma? where does it present anatomically and geographically? what populations?
- neoplasm of Bcells
- affects jaw
- central Africa, new Guniea
- young children
64
what 3 things is Burkitt's assoc with?
1. early EBV inf
2. activation of C-MYC: under Ig promoter :: overexpression
3. malaria: supresses typical immune response
65
Burkitt's lymphoma can/can't be cured if caught early.
can
| 80% cure rate
66
is Burkitt's always assoc with EBV?
no, bc only 20% of pts have EBV assoc outside of Africa
67
where is the assoc bw nasopharyngeal Cx and EBV highest? why?
southern China
| due to high salt diet from the fishies they eat
68
is nasopharyngeal Cx survivable? how does it present?
lump in neck
| nope, at best 60% live past 10y
69
what are other disease assoc with EBV that aren't confirmed, but suspected?
Hodgkin's Lymphoma
| MS
70
what does HHV-8 "cause"? why the air quotes?
it "causes" Kaposi's Sarcoma
| air quotes bc it is "necessary but not sufficient" to cause KS (95% of tumors KS +, 80% seropositive)
71
what pt pop is KS common in?
AIDS
72
where do the KS tumors occur? what cell does it infect?
lining of lymphatic system
| Bcell
73
what are the types of KS? what is the immune-loss mechanism?
1. Classical: Mediterranean; no sex // being old
| 2. AIDS: umm....gays; sex // AIDS
74
HHV-8 is present/not present in what secretions?
not in vag and jizz
in spit
:: get from rimming
75
what is the incubation period of HHV-8 before you get KS?
10 years
76
symptoms of HHV-8
95% asymptomatic
| still can be mild when symptomatic
77
Tx in AIDS pts for HHV-8?
- symptomatic
- treat tumor (resection, chemo)
- treat HIV
- can't spf treat virus
78
what are the Bcell abnormalities linked to HHV-8 that we need to know exist?
Primary Effusion Lymphoma
| Multicentric Castleman's Disease
79
why can't antivirals cure herp or treat the assoc Cx?
they inhibit virus replication when virus is active :: can't work when latent
and Cx is caused from latency NOT the infection
80
EBV v. CMV
both: cause mono, have latency, post-transplant disorders,
CMV: sex transmitted, congenital presentation, ALWAYS heterophile/Monospot (-)
EBV: oncogenic
